JTC-801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3-kinase/protein kinase B signalling pathway
The global rise in liver cancer mortality may be linked to the aggressive progression of the disease. Signal transduction via G-protein-coupled receptors (GPCRs) influences several cancer-related processes, including cell invasion, migration, and vascular remodeling. JTC-801, an innovative GPCR antagonist, has shown promising anticancer effects in adenocarcinoma and osteosarcoma cells. In this study, the impact of JTC-801 on the proliferation and migration of hepatoblastoma Hep G2 cells was examined. The Cell Counting Kit-8 assay demonstrated that JTC-801 significantly suppressed Hep G2 cell growth. Additionally, in a Transwell assay, JTC-801 markedly inhibited cell invasion and migration. Treatment with JTC-801 also resulted in decreased expression of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and increased levels of pro-apoptotic proteins active caspase-3 and apoptosis regulator BAX in Hep G2 cells. Moreover, JTC-801 inhibited the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in these cells. Consequently, this study suggests that JTC-801 can induce apoptosis in Hep G2 cells through PI3K/AKT pathway modulation, positioning JTC-801 as a potential new therapeutic target for liver cancer treatment.